Liquid Biopsy Detects Early Molecular Response and Predicts Benefit to First-Line Chemotherapy plus Cetuximab in Metastatic Colorectal Cancer: PLATFORM-B Study


Por: Vidal J., Fernández-Rodríguez M.C., Casadevall D., García-Alfonso P., Páez D., Guix M., Alonso V., Cano M.T., Santos C., Durán G., Elez E., Manzano J.L., Garcia-Carbonero R., Ferreiro R., Losa F., Pineda E., Sastre J., Rivera F., Bellosillo B., Tabernero J., Aranda E., Salazar R., Montagut C.

Publicada: 1 ene 2023
Resumen:
PURPOSE: Chemotherapy plus anti-EGFR is standard first-line therapy in RAS wild-type (wt) metastatic colorectal cancer (mCRC), but biomarkers of early response are clinically needed. We aimed to define the utility of ctDNA to assess early response in patients with mCRC receiving first-line anti-EGFR therapy. EXPERIMENTAL DESIGN: Prospective multicentric study of tissue patients with RAS wt mCRC treated with first-line chemotherapy plus cetuximab undergoing sequential liquid biopsies. Baseline and early (C3) ctDNA were analyzed by NGS. Trunk mutations were assessed as surrogate marker of total tumor burden. RAS/BRAF/MEK/EGFR-ECD were considered mutations of resistance. ctDNA results were correlated with clinical outcome. RESULTS: One hundred patients were included. ctDNA was detected in 72% of patients at baseline and 34% at C3. Decrease in ctDNA trunk mutations correlated with progression-free survival (PFS; HR, 0.23; P = 0.001). RAS/BRAF were the only resistant mutations detected at C3. An increase in the relative fraction of RAS/BRAF at C3 was followed by an expansion of the RAS clone until PD, and was associated with shorter PFS (HR, 10.5; P < 0.001). The best predictor of response was the combined analysis of trunk and resistant mutations at C3. Accordingly, patients with "early molecular response" (decrease in trunk and decrease in resistant mutations) had better response (77.5% vs. 25%, P = 0.008) and longer PFS (HR, 0.18; P < 0.001) compared with patients with "early molecular progression" (increase in trunk and/or increase in resistant mutations). CONCLUSIONS: ctDNA detects early molecular response and predicts benefit to chemotherapy plus cetuximab. A comprehensive NGS-based approach is recommended to integrate information on total disease burden and resistant mutations. See related commentary by Eluri et al., p. 302. ©2022 American Association for Cancer Research.

Filiaciones:
Vidal J.:
 Medical Oncology Department, Hospital del Mar, Institut Mar Investigacions Mèdiques (IMIM), Universitat Pompeu Fabra, Barcelona, Spain

Fernández-Rodríguez M.C.:
 Pathology Department, Hospital del Mar-IMIM, Barcelona, Spain

Casadevall D.:
 Medical Oncology Department, Hospital del Mar, Institut Mar Investigacions Mèdiques (IMIM), Universitat Pompeu Fabra, Barcelona, Spain

García-Alfonso P.:
 Medical Oncology Department, Hospital Gregorio MarañónMadrid, Spain

Páez D.:
 Medical Oncology Department, H. Santa Creu i Sant Pau, Barcelona, Spain

Guix M.:
 Medical Oncology Department, Hospital del Mar, Institut Mar Investigacions Mèdiques (IMIM), Universitat Pompeu Fabra, Barcelona, Spain

Alonso V.:
 Medical Oncology Department, H. Miguel Servet, Zaragoza, Spain

Cano M.T.:
 Medical Oncology Department, IMIBIC, Reina Sofía Hospital, University of CordobaCordoba, Spain

Santos C.:
 Medical Oncology Department, Catalan Institute of Oncology (ICO), Bellvitge Biomedical Research Institute (IDIBELL)-CIBERONC, Barcelona, Spain

Durán G.:
 Unidad de Gestión Clínica Intercentros de Oncología Médica, Hospitales Universitarios Regional y Virgen de la Victoria, IBIMA, Málaga, Spain

Elez E.:
 Medical Oncology Department, Vall d'Hebron Institute of Oncology (VHIO), Universitat Autònoma de Barcelona, Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain

Manzano J.L.:
 Medical Oncology Department, ICO, H. Germans Trias i Pujol, Barcelona, Spain

Garcia-Carbonero R.:
 Medical Oncology Department, Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), UCM, Hospital Universitario 12 de OctubreMadrid, Spain

Ferreiro R.:
 Medical Oncology Department, Hospital Ramón y CajalMadrid, Spain

Losa F.:
 Medical Oncology Department, Hospital Sant Joan Despí - Moisès Broggi, Spain

Pineda E.:
 Medical Oncology Department Hospital Clínic, Barcelona, Spain

Sastre J.:
 Medical Oncology Department, Hospital Universitario Clínico San CarlosMadrid, Spain

Rivera F.:
 Medical Oncology Department Hospital Marqués de Valdecilla, IDIVALSantander, Spain

Bellosillo B.:
 Pathology Department, Hospital del Mar-IMIM, Barcelona, Spain

Tabernero J.:
 Medical Oncology Department, Vall d'Hebron Institute of Oncology (VHIO), Universitat Autònoma de Barcelona, Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain

Aranda E.:
 Medical Oncology Department, IMIBIC, Reina Sofía Hospital, University of CordobaCordoba, Spain

Salazar R.:
 Medical Oncology Department, Catalan Institute of Oncology (ICO), Bellvitge Biomedical Research Institute (IDIBELL)-CIBERONC, Barcelona, Spain

Montagut C.:
 Medical Oncology Department, Hospital del Mar, Institut Mar Investigacions Mèdiques (IMIM), Universitat Pompeu Fabra, Barcelona, Spain
ISSN: 10780432
Editorial
AMER ASSOC CANCER RESEARCH, 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 29 Número: 2
Páginas: 379-388
WOS Id: 000922091900001
ID de PubMed: 36074154
imagen Green Submitted, All Open Access; Green

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